Vitamin K1 for Atherosclerosis

Vitamin K1 is unproven for atherosclerosis: the largest trial in people without kidney disease found it did not slow coronary artery calcification overall, and no trial has been designed to test heart attacks or strokes. That trial gave 388 healthy older men and postmenopausal women a multivitamin with 500 mcg of phylloquinone a day, or the multivitamin alone, for 3 years. Coronary calcium scores rose by a mean of 27 points with vitamin K1 and 37 without, which was not a significant difference; less progression appeared only in subgroups, which the authors called hypothesis-generating (Shea 2009).

In 154 people with diabetes, 10 mg a day for 3 months did not change coronary calcification activity on PET scans (Bellinge 2022a); fewer new calcifying spots appeared only in a post hoc analysis (Bellinge 2022b). In haemodialysis, a placebo-controlled pilot found no slowing (Holden 2023), while a small open-label trial reported slower aortic calcification (Saritas 2022) and a small trial of intravenous vitamin K1 showed only a non-significant trend (Macias-Cervantes 2025). Large diet studies link more vitamin K1, mostly from leafy vegetables, with fewer atherosclerotic events (Bellinge 2021; Dupuy 2026), but others found no link (Haugsgjerd 2020; Geleijnse 2004), and a 2026 review concluded that no form of vitamin K has been shown to reduce cardiovascular events or deaths (Brandenburg 2026).

Matrix Gla protein (MGP), present in vascular smooth muscle, may help reduce abnormal calcification, and vitamin K is the cofactor for the enzyme that makes vitamin K-dependent proteins work (NIH ODS). MGP acts as a calcification inhibitor only once it is carboxylated, and both phylloquinone (K1) and menaquinones (K2) can do this; a critical review found that claims of unique heart benefits for K2 are not supported by the intervention trials (Shea 2021).

Vitamin K1 supplements reliably shift the marker. In older adults, 500 mcg a day for 3 years lowered plasma uncarboxylated MGP by 345 pmol/L, against 40 pmol/L without it (P < 0.0001) (Shea 2011). In dialysis, 10 mg three times a week cut dephospho-uncarboxylated MGP (dp-ucMGP) by 86% (Holden 2023), and a meta-analysis found vitamin K1 lowered dp-ucMGP more than K2 (Andrian 2023).

A better marker did not mean slower calcification. In the 3-year trial, the fall in uncarboxylated MGP was not associated with the change in coronary calcium (P = 0.44), and the marker did not differ by calcium score (Shea 2011). In dialysis, the same improvement in vitamin K status came with no difference in coronary calcium progression (Holden 2023), and a meta-analysis of dialysis trials found no proven benefit on calcification scores (Andrian 2023).

Calcium scans are also only part of atherosclerosis. Prevention guidelines put a healthy lifestyle first, and statins, blood pressure control, diabetes care and stopping smoking at the centre of treatment; coronary calcium scanning can help guide those decisions (Arnett 2019).

The trial in healthy older adults used 500 mcg of phylloquinone a day in a multivitamin with vitamin D and calcium (Shea 2009; NIH ODS). The diabetes trial used 10 mg a day (Bellinge 2022a). Dialysis trials used 10 mg three times a week (Holden 2023) or 5 mg three times a week by mouth (Saritas 2022), and one gave 10 mg intravenously after each session (Macias-Cervantes 2025), which is a drug treatment, not a supplement.

For comparison, the adequate intake for all vitamin K is 120 mcg a day for men and 90 mcg for women, and no upper limit has been set because no adverse effects from food or supplements have been reported (NIH ODS). Supplements contain phylloquinone or phytonadione, a synthetic form of vitamin K1, and multivitamins typically provide less than 75% of the Daily Value (NIH ODS).

The 3-year trial of 500 mcg a day in 388 healthy older adults found no difference in coronary calcium progression in its main analysis. Less progression appeared in participants who took at least 85% of their doses (P = 0.03) and in those who already had calcification, by 6% (P = 0.04) (Shea 2009). A later post hoc analysis found that among participants taking blood pressure medicine, calcium rose by 5 AU with vitamin K1 and 44 AU with placebo (P < 0.01) (Shea 2013).

In 154 adults with diabetes and coronary calcification, 10 mg a day for 3 months did not change coronary calcification activity on 18F-sodium fluoride PET (mean difference 0.00), and no serious adverse effects were reported (Bellinge 2022a). A post hoc analysis of the same trial found fewer new calcifying lesions in the coronary arteries (OR 0.35, 95% CI 0.16-0.78) and aorta (OR 0.27), and the authors called for longer trials to test it (Bellinge 2022b). In 181 postmenopausal women, of whom 108 were analysed, a 3-year supplement with vitamin K1, minerals and vitamin D preserved carotid artery elasticity compared with placebo, but carotid wall thickness did not differ (Braam 2004).

People on dialysis often lack vitamin K and calcify quickly, which makes them the group where the idea has been tested hardest. In the placebo-controlled iPACK-HD pilot, 86 patients were randomised to 10 mg three times a week or placebo for 12 months; vitamin K status improved, but coronary calcium progressed the same in both groups (Holden 2023). In the open-label VitaVasK trial, stopped early with 40 of 60 patients analysed, 5 mg three times a week for 18 months slowed thoracic aortic calcification by 56% (p = .039), while the 68% slower coronary progression was not significant (P = .072) (Saritas 2022). In 60 Mexican haemodialysis patients, calcium progressed in 20.8% with intravenous vitamin K1 against 44% on placebo, a difference that was not statistically significant (RR 0.45, 95% CI 0.18-1.15), although median scores at 12 months were 78.5 vs 344 AU (p = 0.05) (Macias-Cervantes 2025).

Pooled results are modest. A meta-analysis of 13 vitamin K trials found 9.1% less vascular calcification (95% CI -17.7 to -0.5) with substantial heterogeneity (Lees 2019), and one of 14 trials found a small slowing of coronary calcium (P = 0.04) (Li 2023); both pooled K1 and K2. In chronic kidney disease, meta-analyses found no significant change in calcification scores (Geng 2022) and no effect on mortality (Andrian 2023). A systematic review of nine trials concluded that vitamin K does not consistently prevent progression of calcification, atherosclerosis or arterial stiffness, with possible benefit in people who already have calcification (Vlasschaert 2020). See chronic kidney disease for the wider evidence in that group.

In the Danish Diet, Cancer and Health study of 53,372 adults followed for a median of 21 years, the highest vitamin K1 intakes went with a 21% lower risk of atherosclerotic cardiovascular disease hospitalisation (HR 0.79, 95% CI 0.74-0.84) (Bellinge 2021). In 112,111 UK Biobank participants, higher vitamin K1 intakes were linked to 7-10% lower risk, with no advantage beyond moderate intakes (HR 0.90, 95% CI 0.85-0.95, for the middle vs lowest intake group) (Dupuy 2026). In 1,436 community-dwelling older women, those eating about 119 mcg a day had 5.6% thinner carotid artery walls and fewer atherosclerotic events (HR 0.71) than those eating about 49 mcg (Dupuy 2025).

Other cohorts found nothing. Vitamin K1 intake was not linked to coronary heart disease in Norway (HR 0.92, 95% CI 0.54-1.57) (Haugsgjerd 2020) or in the Rotterdam Study (Geleijnse 2004), nor to coronary calcium in 807 US soldiers (Villines 2005). In 40,087 US men, the link vanished after adjusting for the rest of the diet, suggesting vitamin K1 marks a healthy eating pattern (Erkkilä 2007). A meta-analysis found a small pooled association with coronary heart disease (HR 0.92, 95% CI 0.84-0.99, four studies) but stressed that causality cannot be established (Chen 2019).

No vitamin K1 trial has had heart attacks, strokes or deaths as its main outcome, and the trial in healthy older adults ran only 3 years with a null primary result. Most positive findings need confirming in blinded, placebo-controlled trials with oral doses. The 2026 review judged vitamin K1 the more consistent of the two forms on imaging, especially in dialysis with intensive dosing, but still clinically unproven (Brandenburg 2026). For the menaquinone trials, see vitamin K2 for atherosclerosis.

Vitamin K1 was well tolerated in these trials: no serious adverse effects with 10 mg a day for 3 months (Bellinge 2022a), no treatment-related adverse events over 18 months in dialysis (Saritas 2022), and a dialysis meta-analysis judged vitamin K safe (Andrian 2023). No upper limit has been set for vitamin K (NIH ODS). This applies to oral doses: injected vitamin K1 is a prescription drug whose label carries a boxed warning that severe reactions, including deaths, have occurred during and immediately after intravenous injection (DailyMed).

The serious risk is with blood thinners that work against vitamin K. Vitamin K can have a serious and potentially dangerous interaction with warfarin, phenprocoumon and acenocoumarol, and people taking them need a consistent vitamin K intake because sudden changes can increase or decrease the drug's effect (NIH ODS). Steady intake managed by the clinic is the goal: in 200 patients on phenprocoumon, adding 100 mcg of vitamin K a day did not significantly increase time in the target INR range (89.5% vs 85.5%), though more patients reached maximal INR stability (RR 1.8) (Rombouts 2007). The site's guide to blood thinners and supplements covers other combinations.

Vitamin K antagonists are the one serious interaction. Antibiotics can reduce vitamin K made by gut bacteria; bile acid sequestrants such as cholestyramine and colestipol can reduce absorption of vitamin K; and orlistat can reduce fat-soluble vitamin absorption and, with warfarin, may raise prothrombin time (NIH ODS).